There has been a great deal of interest in the SLC26 gene family largely due to the fact that the SLC26A2, SLC26A3, and SLC26A4 genes have been recognized as disease genes mutated in different pathophysiological states. Recently, the transporter SLC26A7 was identified, abundant expression in the kidney revealed, and it was shown to mediate CI/base exchange. However, several aspects of its normal physiological function and its possible involvement in pathophysiological states remain unclear. [unreadable] There are three major aims of this proposal. First, isoform-specific antibodies to SLC26A7 and the alternatively spliced SLC26A7.2 will be generated and nephron localization of the proteins characterized by immunofluorescence microscopy. Additionally, using Northern blot analysis and PCR/RT-PCR the putative mouse SLC26A7.2 ortholog will be identified. Next, membrane targeting for each splice variant will be examined by immunofluorescence and confocal microscopy of transfected, epitope-tagged constructs. [unreadable] Last, using immunoprecipitation and pull-down experiments association of SLC26A7 with accessory proteins through interaction at its C-terminal PDZ-interacting motif will be examined. [unreadable] [unreadable] [unreadable]